Zhang Song, Chen Anqi, Chen Xiaolu
Department of Dermatology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Department of Neurology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Front Physiol. 2021 Mar 17;12:619904. doi: 10.3389/fphys.2021.619904. eCollection 2021.
Vascular endothelial growth factor (VEGF) plays a pivotal role in regulating cerebral angiogenesis after stroke. Meanwhile, excessive VEGF expression induces increased microvascular permeability in brain, probably leading to neurological deterioration. Therefore, the appropriate level of VEGF expression is significant to the recovery of brain exposed to stroke. In this work, we demonstrate that microRNA-150 (miR-150) and its predicted target MYB form a negative feedback loop to control the level of post-stroke VEGF expression. Repression of MYB leads to decreased expression of miR-150 in brain microvascular endothelial cells (BMVECs) exposed to oxygen glucose deprivation (OGD), thus miR-150 was predicted to be down-regulated by MYB. Moreover, MYB was confirmed to be a direct target of miR-150 by using dual luciferase reporter assay. In our previous work, we have validated VEGF as another direct target of miR-150. Therefore, MYB participates in regulation of VEGF via miR-150 under OGD, forming a feedback loop with miR-150. We also find that high levels of miR-150 inhibitors combined with MYB silence contribute to further enhancement of VEGF expression in BMVECs in response to OGD. These observations suggest that the feedback loop comprised of miR-150 and MYB, which is a pivotal endogenous epigenetic regulation to control the expression levels of VEGF in BMVECs subjected to OGD.
血管内皮生长因子(VEGF)在中风后调节脑内血管生成中起关键作用。同时,VEGF的过度表达会导致脑内微血管通透性增加,可能导致神经功能恶化。因此,VEGF表达的适当水平对中风后脑的恢复至关重要。在这项研究中,我们证明了微小RNA-150(miR-150)及其预测靶点MYB形成了一个负反馈环,以控制中风后VEGF的表达水平。在暴露于氧糖剥夺(OGD)的脑微血管内皮细胞(BMVECs)中,抑制MYB会导致miR-150表达降低,因此预测miR-150受MYB下调。此外,通过双荧光素酶报告基因检测证实MYB是miR-150的直接靶点。在我们之前的研究中,我们已验证VEGF是miR-150的另一个直接靶点。因此,在OGD条件下,MYB通过miR-150参与VEGF的调控,与miR-150形成一个反馈环。我们还发现,高水平的miR-150抑制剂与MYB沉默相结合,有助于进一步增强BMVECs在OGD刺激下VEGF的表达。这些观察结果表明,由miR-150和MYB组成的反馈环,是在OGD条件下控制BMVECs中VEGF表达水平的关键内源性表观遗传调控机制。